Identifying sources of D-serine in Caenorhabditis elegans and their impact on behavior

2021 ◽  
Author(s):  
Tian A. Qiu ◽  
Harvey M. Andersen ◽  
Nissa J. Larson ◽  
Nathan E. Schroeder ◽  
Jonathan V. Sweedler
Keyword(s):  
Caenorhabditis Elegans ◽  
Sequence Similarity ◽  
Serine Racemase ◽  
Behavioral Changes ◽  
C Elegans ◽  
Aspartate Receptor ◽  
Two Factors ◽  
Locomotion Behavior ◽  
Culturing Conditions

Free D-serine (D-Ser) is a potent co-agonist of the N-methyl-D-aspartate receptor (NMDAR) in glutamate neurotransmission and regulates NMDAR functions in the nervous system. Serine racemases convert L-serine to D-Ser and are believed to be the major source of D-Ser in animals. In Caenorhabditis elegans, a knockout of the serine racemase serr-1 results in behavioral changes, but the level of D-Ser is unaffected. By growing C. elegans on peptone-free nematode growth medium (PF-NGM), we delineated the sources of D-Ser, both exogenous from peptone in culturing media and endogenous from the serine racemase serr-1, and a potential serine/aspartate racemase candidate, Y51H7C.9, identified by sequence similarity network analysis. We also discovered a new serine dehydratase (aka serine ammonia-lyase), K01C8.1, in C. elegans. We identified the serr-1 knockout and PF-NGM culturing conditions as two independent factors that impact C. elegans locomotion behavior after off-food, both short-term and long-term, and no interactions were found between the two factors.

lag-1, a gene required for lin-12 and glp-1 signaling in Caenorhabditis elegans, is homologous to human CBF1 and Drosophila Su(H)

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1373-1383 ◽  
Author(s):  
S. Christensen ◽  
V. Kodoyianni ◽  
M. Bosenberg ◽  
L. Friedman ◽  
J. Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Binding Sites ◽  
Feedback Loop ◽  
Target Genes ◽  
Sequence Similarity ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Downstream Target ◽  
Binding Factor ◽  
Flanking Regions

The homologous receptors LIN-12 and GLP-1 mediate diverse cell-signaling events during development of the nematode Caenorhabditis elegans. These two receptors appear to be functionally interchangeable and have sequence similarity to Drosophila Notch. Here we focus on a molecular analysis of the lag-1 gene (lin-12 -and glp-1), which plays a central role in LIN-12 and GLP-1-mediated signal transduction. We find that the predicted LAG-1 protein is homologous to two DNA-binding proteins: human C Promoter Binding Factor (CBF1) and Drosophila Suppressor of Hairless (Su(H)). Furthermore, we show that LAG-1 binds specifically to the DNA sequence RTGGGAA, previously identified as a CBF-1/Su(H)-binding site. Finally, we report that the 5′ flanking regions and first introns of the lin-12, glp-1 and lag-1 genes are enriched for potential LAG-1-binding sites. We propose that LAG-1 is a transcriptional regulator that serves as a primary link between the LIN-12 and GLP-1 receptors and downstream target genes in C. elegans. In addition, we propose that LAG-1 may be a key component of a positive feedback loop that amplifies activity of the LIN-12/GLP-1 pathway.

Xenon Acts by Inhibition of Non–N -methyl-d-aspartate Receptor–mediated Glutamatergic Neurotransmission in Caenorhabditis elegans 

2005 ◽  
Vol 103 (3) ◽  
pp. 508-513 ◽  
Author(s):  
Peter Nagele ◽  
Laura B. Metz ◽  
C Michael Crowder
Keyword(s):  
Nitrous Oxide ◽  
Caenorhabditis Elegans ◽  
Nmda Receptor ◽  
Glutamate Receptor ◽  
Glutamatergic Transmission ◽  
Wild Type ◽  
C Elegans ◽  
Aspartate Receptor ◽  
Nmda Glutamate Receptor ◽  
Response Transformation

Background Electrophysiologic experiments in rodents have found that nitrous oxide and xenon inhibit N-methyl-D-aspartate (NMDA)-type glutamate receptors. These findings led to the hypothesis that xenon and nitrous oxide along with ketamine form a class of anesthetics with the identical mechanism, NMDA receptor antagonism. Here, the authors ask in Caenorhabditis elegans whether xenon, like nitrous oxide, acts by a NMDA receptor-mediated mechanism. Methods Xenon:oxygen mixtures were delivered into sealed chambers until the desired concentration was achieved. The effects of xenon on various behaviors were measured on wild-type and mutant C. elegans strains. Results With an EC50 of 15-20 vol% depending on behavioral endpoint, xenon altered C. elegans locomotion in a manner indistinguishable from that of mutants in glutamatergic transmission. Xenon reduced the frequency and duration of backward locomotion without altering its speed or other behaviors tested. Mutation of glr-1, encoding a non-NMDA glutamate receptor subunit, abolished the behavioral effects of xenon; however, mutation of nmr-1, which encodes the pore-forming subunit of an NMDA glutamate receptor previously shown to be required for nitrous oxide action, did not significantly alter xenon response. Transformation of the glr-1 mutant with the wild-type glr-1 gene partially restored xenon sensitivity, confirming that glr-1 was necessary for the full action of xenon. Conclusions Xenon acts in C. elegans to alter locomotion through a mechanism requiring the non-NMDA glutamate receptor encoded by glr-1. Unlike for the action of nitrous oxide in C. elegans, the NMDA receptor encoded by nmr-1 is not essential for sensitivity to xenon.

scholarly journals Interspecies RNA Interactome of Pathogen and Host in a Heritable Defensive Strategy

2021 ◽  
Vol 12 ◽  
Author(s):  
Marcela Legüe ◽  
Blanca Aguila ◽  
Andrea Calixto
Keyword(s):  
Behavioral Changes ◽  
Defensive Strategy ◽  
C Elegans ◽  
Mrna Targets ◽  
Bacterial Rna ◽  
Triggering Conditions ◽  
Short And Long Term ◽  
Rna Interaction ◽  
Pathogen Avoidance

Communication with bacteria deeply impacts the life history traits of their hosts. Through specific molecules and metabolites, bacteria can promote short- and long-term phenotypic and behavioral changes in the nematode Caenorhabditis elegans. The chronic exposure of C. elegans to pathogens promotes the adaptive behavior in the host’s progeny called pathogen-induced diapause formation (PIDF). PIDF is a pathogen avoidance strategy induced in the second generation of animals infected and can be recalled transgenerationally. This behavior requires the RNA interference machinery and specific nematode and bacteria small RNAs (sRNAs). In this work, we assume that RNAs from both species co-exist and can interact with each other. Under this principle, we explore the potential interspecies RNA interactions during PIDF-triggering conditions, using transcriptomic data from the holobiont. We study two transcriptomics datasets: first, the dual sRNA expression of Pseudomonas aeruginosa PAO1 and C. elegans in a transgenerational paradigm for six generations and second, the simultaneous expression of sRNAs and mRNA in intergenerational PIDF. We focus on those bacterial sRNAs that are systematically overexpressed in the intestines of animals compared with sRNAs expressed in host-naïve bacteria. We selected diverse in silico methods that represent putative mechanisms of RNA-mediated interspecies interaction. These interactions are as follows: heterologous perfect and incomplete pairing between bacterial RNA and host mRNA; sRNAs of similar sequence expressed in both species that could mimic each other; and known or predicted eukaryotic motifs present in bacterial transcripts. We conclude that a broad spectrum of tools can be applied for the identification of potential sRNA and mRNA targets of the interspecies RNA interaction that can be subsequently tested experimentally.

scholarly journals An opioid-like system regulating feeding behavior in C. elegans

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Mi Cheong Cheong ◽  
Alexander B Artyukhin ◽  
Young-Jai You ◽  
Leon Avery
Keyword(s):  
Caenorhabditis Elegans ◽  
Feeding Behavior ◽  
Opioid Receptors ◽  
Motor Neurons ◽  
Sequence Similarity ◽  
Rnai Screen ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
C Elegans ◽  
Opioid Neuropeptides

Neuropeptides are essential for the regulation of appetite. Here we show that neuropeptides could regulate feeding in mutants that lack neurotransmission from the motor neurons that stimulate feeding muscles. We identified nlp-24 by an RNAi screen of 115 neuropeptide genes, testing whether they affected growth. NLP-24 peptides have a conserved YGGXX sequence, similar to mammalian opioid neuropeptides. In addition, morphine and naloxone respectively stimulated and inhibited feeding in starved worms, but not in worms lacking NPR-17, which encodes a protein with sequence similarity to opioid receptors. Opioid agonists activated heterologously expressed NPR-17, as did at least one NLP-24 peptide. Worms lacking the ASI neurons, which express npr-17, did not response to naloxone. Thus, we suggest that Caenorhabditis elegans has an endogenous opioid system that acts through NPR-17, and that opioids regulate feeding via ASI neurons. Together, these results suggest C. elegans may be the first genetically tractable invertebrate opioid model.

Caenorhabditis elegans Learning and Memory

2019 ◽  
Author(s):  
James S.H. Wong ◽  
Catharine H. Rankin
Keyword(s):  
Carbon Dioxide ◽  
Caenorhabditis Elegans ◽  
Classical Conditioning ◽  
Learning And Memory ◽  
Long Term Memory ◽  
Context Conditioning ◽  
Term Memory ◽  
C Elegans

The nematode, Caenorhabditis elegans (C. elegans), is an organism useful for the study of learning and memory at the molecular, cellular, neural circuitry, and behavioral levels. Its genetic tractability, transparency, connectome, and accessibility for in vivo cellular and molecular analyses are a few of the characteristics that make the organism such a powerful system for investigating mechanisms of learning and memory. It is able to learn and remember across many sensory modalities, including mechanosensation, chemosensation, thermosensation, oxygen sensing, and carbon dioxide sensing. C. elegans habituates to mechanosensory stimuli, and shows short-, intermediate-, and long-term memory, and context conditioning for mechanosensory habituation. The organism also displays chemotaxis to various chemicals, such as diacetyl and sodium chloride. This behavior is associated with several forms of learning, including state-dependent learning, classical conditioning, and aversive learning. C. elegans also shows thermotactic learning in which it learns to associate a particular temperature with the presence or absence of food. In addition, both oxygen preference and carbon dioxide avoidance in C. elegans can be altered by experience, indicating that they have memory for the oxygen or carbon dioxide environment they were reared in. Many of the genes found to underlie learning and memory in C. elegans are homologous to genes involved in learning and memory in mammals; two examples are crh-1, which is the C. elegans homolog of the cAMP response element-binding protein (CREB), and glr-1, which encodes an AMPA glutamate receptor subunit. Both of these genes are involved in long-term memory for tap habituation, context conditioning in tap habituation, and chemosensory classical conditioning. C. elegans offers the advantage of having a very small nervous system (302 neurons), thus it is possible to understand what these conserved genes are doing at the level of single identified neurons. As many mechanisms of learning and memory in C. elegans appear to be similar in more complex organisms including humans, research with C. elegans aids our ever-growing understanding of the fundamental mechanisms of learning and memory across the animal kingdom.

Long-term sediment exposure to ZnO nanoparticles induces oxidative stress in Caenorhabditis elegans

2019 ◽  
Vol 6 (8) ◽  
pp. 2602-2614 ◽  
Author(s):  
Chi-Wei Huang ◽  
Shang-Wei Li ◽  
Vivian Hsiu-Chuan Liao
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Zno Nanoparticles ◽  
Gene Activation ◽  
Benthic Organism ◽  
Zno Nps ◽  
C Elegans ◽  
Sediment Exposure

Long-term sediment exposure to ZnO-NPs induces oxidative stress in benthic organism C. elegans which is mediated by the transcription factor DAF-16/FOXO triggering stress-responsive gene activation.

scholarly journals Embryonic Methamphetamine Exposure Inhibits Methamphetamine Cue Conditioning and Reduces Dopamine Concentrations in Adult N2 Caenorhabditis elegans

2016 ◽  
Vol 38 (2) ◽  
pp. 139-149 ◽  
Author(s):  
Simon N. Katner ◽  
Bethany S. Neal-Beliveau ◽  
Eric A. Engleman
Keyword(s):  
Caenorhabditis Elegans ◽  
Chloride Ions ◽  
Well Test ◽  
Long Term Effects ◽  
Liquid Filtration ◽  
C Elegans ◽  
Embryonic Exposure ◽  
Conditioning Data ◽  
Food Conditioning

Methamphetamine (MAP) addiction is substantially prevalent in today's society, resulting in thousands of deaths and costing billions of dollars annually. Despite the potential deleterious consequences, few studies have examined the long-term effects of embryonic MAP exposure. Using the invertebrate nematode Caenorhabditis elegans allows for a controlled analysis of behavioral and neurochemical changes due to early developmental drug exposure. The objective of the current study was to determine the long-term behavioral and neurochemical effects of embryonic exposure to MAP in C. elegans. In addition, we sought to improve our conditioning and testing procedures by utilizing liquid filtration, as opposed to agar, and smaller, 6-well testing plates to increase throughput. Wild-type N2 C. elegans were embryonically exposed to 50 μM MAP. Using classical conditioning, adult-stage C. elegans were conditioned to MAP (17 and 500 μM) in the presence of either sodium ions (Na+) or chloride ions (Cl-) as conditioned stimuli (CS+/CS-). Following conditioning, a preference test was performed by placing worms in 6-well test plates spotted with the CS+ and CS- at opposite ends of each well. A preference index was determined by counting the number of worms in the CS+ target zone divided by the total number of worms in the CS+ and CS- target zones. A food conditioning experiment was also performed in order to determine whether embryonic MAP exposure affected food conditioning behavior. For the neurochemical experiments, adult worms that were embryonically exposed to MAP were analyzed for dopamine (DA) content using high-performance liquid chromatography. The liquid filtration conditioning procedure employed here in combination with the use of 6-well test plates significantly decreased the time required to perform these experiments and ultimately increased throughput. The MAP conditioning data found that pairing an ion with MAP at 17 or 500 μM significantly increased the preference for that ion (CS+) in worms that were not pre-exposed to MAP. However, worms embryonically exposed to MAP did not exhibit significant drug cue conditioning. The inability of MAP-exposed worms to condition to MAP was not associated with deficits in food conditioning, as MAP-exposed worms exhibited a significant cue preference associated with food. Furthermore, our results found that embryonic MAP exposure reduced DA levels in adult C. elegans, which could be a key mechanism contributing to the long-term effects of embryonic MAP exposure. It is possible that embryonic MAP exposure may be impairing the ability of C. elegans to learn associations between MAP and the CS+ or inhibiting the reinforcing properties of MAP. However, our food conditioning data suggest that MAP-exposed animals can form associations between cues and food. The depletion of DA levels during embryonic exposure to MAP could be responsible for driving either of these processes during adulthood.

scholarly journals Salmonella biofilms program innate immunity for persistence in Caenorhabditis elegans

2019 ◽  
Vol 116 (25) ◽  
pp. 12462-12467 ◽  
Author(s):  
Stuti K. Desai ◽  
Anup Padmanabhan ◽  
Sharvari Harshe ◽  
Ronen Zaidel-Bar ◽  
Linda J. Kenney
Keyword(s):  
Caenorhabditis Elegans ◽  
Temporal Dynamics ◽  
Innate Immune ◽  
Heterologous Host ◽  
C Elegans ◽  
Parasitic Lifestyle ◽  
Induced Changes ◽  
Infectious Form

The adaptive in vivo mechanisms underlying the switch in Salmonella enterica lifestyles from the infectious form to a dormant form remain unknown. We employed Caenorhabditis elegans as a heterologous host to understand the temporal dynamics of Salmonella pathogenesis and to identify its lifestyle form in vivo. We discovered that Salmonella exists as sessile aggregates, or in vivo biofilms, in the persistently infected C. elegans gut. In the absence of in vivo biofilms, Salmonella killed the host more rapidly by actively inhibiting innate immune pathways. Regulatory cross-talk between two major Salmonella pathogenicity islands, SPI-1 and SPI-2, was responsible for biofilm-induced changes in host physiology during persistent infection. Thus, biofilm formation is a survival strategy in long-term infections, as prolonging host survival is beneficial for the parasitic lifestyle.

scholarly journals Transgenerational Diapause as an Avoidance Strategy against Bacterial Pathogens in Caenorhabditis elegans

mBio ◽  
2017 ◽  
Vol 8 (5) ◽  
Author(s):  
M. Fernanda Palominos ◽  
Lidia Verdugo ◽  
Carolaing Gabaldon ◽  
Bernardo Pollak ◽  
Javiera Ortíz-Severín ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Behavioral Change ◽  
Pathogenic Bacteria ◽  
Behavioral Changes ◽  
Survival Strategies ◽  
Information Encoding ◽  
C Elegans ◽  
Two Generations ◽  
And Behavior ◽  
Dauer Larvae

ABSTRACT The dynamic response of organisms exposed to environmental pathogens determines their survival or demise, and the outcome of this interaction depends on the host’s susceptibility and pathogen-dependent virulence factors. The transmission of acquired information about the nature of a pathogen to progeny may ensure effective defensive strategies for the progeny’s survival in adverse environments. Environmental RNA interference (RNAi) is a systemic and heritable mechanism and has recently been linked to antibacterial and antifungal defenses in both plants and animals. Here, we report that the second generation of Caenorhabditis elegans living on pathogenic bacteria can avoid bacterial infection by entering diapause in an RNAi pathway-dependent mechanism. Furthermore, we demonstrate that the information encoding this survival strategy is transgenerationally transmitted to the progeny via the maternal germ line. IMPORTANCE Bacteria vastly influence physiology and behavior, and yet, the specific mechanisms by which they cause behavioral changes in hosts are not known. We use C. elegans as a host and the bacteria they eat to understand how microbes trigger a behavioral change that helps animals to survive. We found that animals faced with an infection for two generations could enter a hibernationlike state, arresting development by forming dauer larvae. Dauers have closed mouths and effectively avoid infection. Animals accumulate information that is transgenerationally transmitted to the next generations to form dauers. This work gives insight on how bacteria communicate in noncanonical ways with their hosts, resulting in long-lasting effects providing survival strategies to the community. IMPORTANCE Bacteria vastly influence physiology and behavior, and yet, the specific mechanisms by which they cause behavioral changes in hosts are not known. We use C. elegans as a host and the bacteria they eat to understand how microbes trigger a behavioral change that helps animals to survive. We found that animals faced with an infection for two generations could enter a hibernationlike state, arresting development by forming dauer larvae. Dauers have closed mouths and effectively avoid infection. Animals accumulate information that is transgenerationally transmitted to the next generations to form dauers. This work gives insight on how bacteria communicate in noncanonical ways with their hosts, resulting in long-lasting effects providing survival strategies to the community.

scholarly journals Patterns of Selection Against Transposons Inferred From the Distribution of Tc1, Tc3 and Tc5 Insertions in the mut-7 Line of the Nematode Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1127-1135
Author(s):  
Carène Rizzon ◽  
Edwige Martin ◽  
Gabriel Marais ◽  
Laurent Duret ◽  
Laurent Ségalat ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Selective Pressure ◽  
Theoretical Models ◽  
Nematode Caenorhabditis Elegans ◽  
Recombination Rates ◽  
Noncoding Regions ◽  
C Elegans ◽  
Coding Regions ◽  
A Genome ◽  
Two Factors

Abstract To identify the factors (selective or mutational) that affect the distribution of transposable elements (TEs) within a genome, it is necessary to compare the pattern of newly arising element insertions to the pattern of element insertions that have been fixed in a population. To do this, we analyzed the distribution of recent mutant insertions of the Tc1, Tc3, and Tc5 elements in a mut-7 background of the nematode Caenorhabditis elegans and compared it to the distribution of element insertions (presumably fixed) within the sequenced genome. Tc1 elements preferentially insert in regions with high recombination rates, whereas Tc3 and Tc5 do not. Although Tc1 and Tc3 both insert in TA dinucleotides, there is no clear relationship between the frequency of insertions and the TA dinucleotide density. There is a strong selection against TE insertions within coding regions: the probability that a TE will be fixed is at least 31 times lower in coding regions than in noncoding regions. Contrary to the prediction of theoretical models, we found that the selective pressure against TE insertions does not increase with the recombination rate. These findings indicate that the distribution of these three transposon families in the genome of C. elegans is determined essentially by just two factors: the pattern of insertions, which is a characteristic of each family, and the selection against insertions within coding regions.

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